Genotoxic effect of meat consumption: A mini review

Pelland-St-Pierre, Laura; Sernoskie, Samantha Christine; Verner, Marc-André; Ho, Vikki

doi:10.1016/j.mrgentox.2021.503311

Cited by 3 publications

(2 citation statements)

References 66 publications

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“…Red meat and processed meat are well documented risk factors for colorectal cancer ( 23 ) due to their genotoxic effects ( 30 ). Despite this, red meat consumption was not shown to be a risk factor for early-onset colorectal adenomas and results were mixed for EOCRC.…”

Section: Discussionmentioning

confidence: 99%

Diet as a Risk Factor for Early-Onset Colorectal Adenoma and Carcinoma: A Systematic Review

et al. 2022

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BackgroundColorectal cancer in adults 50 years old and younger is increasing in incidence worldwide. Diet may be a modifiable risk factor. The objective of this study was to examine evidence regarding the association between diet and the risk of developing early-onset colorectal cancer (EOCRC) and early-onset colorectal adenomas in young adults.MethodsPUBMED, Web of Science, and Embase were systematically searched for studies examining dietary intake as a risk factor for EOCRC and early-onset colorectal adenomas. Results were synthesized narratively due to the heterogeneity of the studies.ResultsOf the 415 studies identified, ten met the inclusion criteria. Of these ten studies, four provided data on dietary risk factors for early-onset colorectal adenomas and six provided data on dietary risk factors for EOCRC. The four studies that measured colorectal adenoma occurrence reported an increased incidence with high sugar sweetened beverage intake, a higher pro-inflammatory diet, a higher Western diet score and higher sulfur microbial diet score. A protective effect against early-onset colorectal adenomas was observed in those who had a higher Prudent diet score or higher adherence to other health dietary approaches (Dietary Approaches to Stop Hypertension, Alternative Healthy Eating Index-2010, or the alternative Mediterranean diet). Those who consumed large amounts of deep-fried foods, refined foods, followed a high fat diet, consumed large amounts of sugary drinks and desserts, and had low folate and fiber consumption had a significantly higher occurrence of EOCRC. A protective effect against EOCRC was observed for those who consumed more fruits and vegetables, high amounts of micronutrients and those who adhered to a vegetarian diet.ConclusionsThe results of this study reveal various dietary habits may be risk factors or protective against early-onset colorectal cancer and adenomas. Future research should focus on large prospective cohort studies with long-term follow-up to confirm published results and further examine whether differences in diet quality are associated with EOCRC risk.

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Section: Discussionmentioning

confidence: 99%

Diet as a Risk Factor for Early-Onset Colorectal Adenoma and Carcinoma: A Systematic Review

et al. 2022

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“…The epidemiological data has confirmed the same, but the underlying mechanism for mechanisms of genotoxicity and how cancer is induced is still unclear, particularly the extent to which DNA damage is caused. The literature studies suggest that meat consumption can cause DNA breaks, adduct formation (Pelland-St-Pierre et al 2021 ).…”

Section: Environmental Mutagens As Dna Damage Activators Enhancing Carcinogenesismentioning

confidence: 99%

Unboxing the molecular modalities of mutagens in cancer

Kumari

Sharma

Advani

et al. 2021

Environ Sci Pollut Res

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Graphical abstract The etiology of the majority of human cancers is associated with a myriad of environmental causes, including physical, chemical, and biological factors. DNA damage induced by such mutagens is the initial step in the process of carcinogenesis resulting in the accumulation of mutations. Mutational events are considered the major triggers for introducing genetic and epigenetic insults such as DNA crosslinks, single- and double-strand DNA breaks, formation of DNA adducts, mismatched bases, modification in histones, DNA methylation, and microRNA alterations. However, DNA repair mechanisms are devoted to protect the DNA to ensure genetic stability, any aberrations in these calibrated mechanisms provoke cancer occurrence. Comprehensive knowledge of the type of mutagens and carcinogens and the influence of these agents in DNA damage and cancer induction is crucial to develop rational anticancer strategies. This review delineated the molecular mechanism of DNA damage and the repair pathways to provide a deep understanding of the molecular basis of mutagenicity and carcinogenicity. A relationship between DNA adduct formation and cancer incidence has also been summarized. The mechanistic basis of inflammatory response and oxidative damage triggered by mutagens in tumorigenesis has also been highlighted. We elucidated the interesting interplay between DNA damage response and immune system mechanisms. We addressed the current understanding of DNA repair targeted therapies and DNA damaging chemotherapeutic agents for cancer treatment and discussed how antiviral agents, anti-inflammatory drugs, and immunotherapeutic agents combined with traditional approaches lay the foundations for future cancer therapies.

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